1. Field of the Invention
The present invention relates generally to implantable cardiac stimulators, such as cardiac pacemakers, cardioverters and defibrillators; and more particularly to fixation mechanisms for the lead/electrode assemblies of implantable cardiac stimulators.
2. Prior Art
The sinoatrial (S-A) node of the human heart acts as the natural pacemaker by which rhythmic electrical excitation is developed and propagated to the atria. In response, the atrial chambers contract, pumping blood into the ventricles. The rhythmic excitation is further propagated through the atrioventricular (A-V) node, which imposes a delay, and then via the conduction system consisting of the bundle of His and the Purkinge fibers to the ventricular myocardium, producing contraction of the ventricles. As a result, the oxygen-depleted blood in the right ventricle is pumped through the pulmonary artery to the lungs, and the oxygenated blood in the left ventricle is pumped through the arteries to the body. The right atrium receives the oxygen-depleted blood from the body via the veins, and the left atrium receives oxygenated blood from the lungs.
The actions repeat in a rhythmic cardiac cycle in which the atrial and ventricular chambers alternately contract and pump, relax and fill. One way valves along the veins, between the chambers in the right side (tricuspid valve) and the left side (mitral valve) of the heart, and at the exits of the right ventricle (pulmonary valve) and left ventricle (aortic valve) prevent backflow of the blood as it moves through the heart and circulatory system.
The S-A node is spontaneously rhythmic, and with a normal excitation and propagation system the heart beats in an organized manner at a regular rate termed sinus rhythm. Disruption of the natural pacing and propagation system as a result of aging or disease is commonly treated by artificial cardiac pacing, in which a cardiac pacemaker is implanted to maintain the desired heart rate.
Implantable artificial cardiac pacemakers, or, more simply, "pacemakers," are designed to operate in one of several different response modes. These include asynchronous, or fixed rate stimulation; inhibited, or stimulation only after a predetermined interval without specified normal cardiac activity; and triggered, or stimulation only in response to specified cardiac activity. All three of these pacemaker types employ, in simplest form, a stimulus generator ("pulse generator") housed in a case and powered by a self-contained battery, and a lead assembly (generally referred to simply as a "lead") having one or more electrodes coupled to conductor(s) for electrical connection to the generator circuitry via a connector built into the case. The pacing electrode is variously referred to as the stimulating cathodic electrode, the stimulating electrode, or merely the cathode, and the indifferent electrode is alternatively referred to as the reference electrode, the anodic electrode, or simply the anode. In fact, however, electrical activity takes place at each electrode during pacing, and the coupling may be such that each electrode acts, at different times, as cathode or anode. The pulse generator and the lead are manufactured and distributed as separate items, the leads being interchangeable with pulse generators of the various types.
Typically, the lead is inserted through the superior vena cava (the great vein which transports unoxygenated blood from the upper part of the body to the right atrium) until the stimulating electrode at the distal end of the lead is brought into proper position within the desired chamber in the right side of the patient's heart. Because it is adapted for intravenous insertion, the lead is sometimes referred to as a "catheter lead"; and because the electrode is adapted to be positioned within the heart, it is often called an "endocardial electrode". The proximal end of the lead is inserted and fastened into the integral connector of the pulse generator case, thereby electrically coupling the stimulating electrode to the pacemaker circuitry within the case. The case in which the pulse generator is housed is implanted in a subcutaneous pouch formed by an incision in the patient's chest. With dual chamber pacemakers, both chambers of the heart may be stimulated and/or sensed using two separate leads, one of which is introduced into the right atrium and the other into the right ventricle.
By appropriately manipulating the lead, the implanting physician positions and, if necessary, repositions the stimulating electrode to assure consistent "capture" of the heart, that is to say, that the patient's heart responds to each stimulus generated by the pacemaker. In essence, the stimulating electrode serves to impress an electric field, resulting from electrical discharge by the pulse generator, on excitable myocardial tissue in the vicinity of that electrode. This is accomplished via an electrical circuit consisting of the pulse generator, the conducting lead, the stimulating electrode, the indifferent electrode, and the volume conductor comprising the patient's body tissue and fluid.
The pacemaker may be arranged for unipolar or bipolar stimulation according to the configuration and location of the indifferent electrode. For unipolar stimulation, the anode is somewhat remote from the heart, typically constituting part of the metal case that houses the pulse generator. Some patients may experience pectoral stimulation as the heart is being paced, a condition attributable to the presence of a large area electrode--the case--in contact with the chest muscle. To alleviate that condition, it is customary to reduce the size of the anode to a small portion of the case itself by coating most of the case with a biologically compatible electrical insulator, such as paralene, leaving only the limited uncoated portion in conductive contact with the body tissue and fluid. This reduction in size of the anode may reduce the effectiveness of the circuit ground (reference potential). For such reasons, the cardiologist or surgeon may prefer to forego the simplicity of unipolar pacing for a particularly sensitive patient, and instead select bipolar pacing. for purposes of pacemaker operation in the latter mode, the lead to be implanted is configured with the cathode and the anode insulatively separated from but in close proximity to one another at the distal end of the lead. Typically, the cathode is located at or near the tip of the lead and the anode is configured as a ring electrode spaced back one half inch or so from the cathode. Each electrode is connected to its own electrically conductive coil within the lead.
The stimulating electric field generated by the pace-maker in the vicinity of the cathode must be of sufficient impulse strength to initiate a so-called "action potential" and depolarization of cells within the excitable tissue, in order to cause and propagate cardiac stimulation. The smallest electrical impulse necessary to initiate such stimulation is referred to as the "stimulation threshold," or simply "threshold".
In practice, the cardiologist or surgeon will set the stimulation level to comfortably exceed the threshold for the particular patient and pacing system. Indeed, since there is invariably an acute but gradual rise in threshold over a period of from about one to four weeks after the pacemaker is implated, it is customary to set the stimulus level initially at about four times that of the threshold measured at implant. The increase in acute threshold is attributable in part to the growth of a fibrotic layer of non-excitable tissue of uneven thickness about the electrode tip in contact with the myocardium, which effectively increases the surface area of the electrode and lowers the current density. Another factor is the inflammation reaction at the tip. The chronic threshold is usually observed about four to eight weeks after implantation.
It is common practice to seek to position the stimulating cathodic electrode at the time of implant at a location within the chamber to be paced which offers the lowest threshold and the greatest mechanical stability. Until the stimulating electrode becomes secured in place as a result of fibrotic growth, a period which depends in large measure on the structure and composition of the electrode, it is subject to dislodgement because of the rhythmic contraction and relaxation of the heart, or even merely as a consequence of general body movements of the patient.
Various electrode fixation mechanisms have been devised since the inception of the artificial pacemaker to secure the lead (and more particularly, the electrode) in place after positioning by the cardiologist or surgeon. Such mechanisms fall into two categories. Some offer passive fixation, by means of non-invasive devices such as pliant barbs (so-called "tines") attached at or near the lead tip to engage the trabeculae within the heart chamber. Others provide more positive fixation, termed "active fixation," of the electrode. The known active fixation mechanisms include corkscrews, hooks, piercing barbs, or other anchoring means arranged at or near the lead tip for penetration of the endocardium upon manipulation of the lead and/or a stylet traversing the lead, following proper positioning of the cathode.
It is a principal object of the present invention to provide a new and improved active fixation mechanism for cardiac stimulating electrodes.
Examples of active fixation mechanisms heretofore proposed include the following. U.S. Patent No. 3,943,936 to Rasor et al., assigned to the same assignee as is the present invention, discloses various means for attaching the stimulating electrode to the myocardium, including spiral retention wires and wire barbs. U.S. Patent Nos. 4,142,530 to Wittkampf, 4,217,913 to Dutcher, and 4,357,946 to Dutcher et al. describe stylet-actuated anchoring means including hooks and corkscrews for catheter electrodes. U.S. Patent No. 4,378,023 to Trabucco discloses anchoring mechanisms in the form of normally recessed pins and hooks which are stylet-deployable to engage the tissue and anchor the electrode. Similarly, U.S. Patent No. 4,233,992 to Bisping describes various forms of fixing hooks normally recessed within the contour of the electrode head for ease of insertion through the vein to place the electrode into desired position, and stylet-pivotable to protrude beyond the electrode head such that upon twisting the lead, the hook engages the heart tissue. Bisping further suggests that the fixing hook or the electrode head be provided with barbs to prevent disengagement of the hook, and also describes alternatives to stylet actuation of the fixing hook.
A serious problem with many of the previous approaches toward active fixation of the lead/electrode is that the anchoring means is permanently deployed, or is not easily retracted to its original position after deployment. Thus, while it may be relatively easy to thread the lead through the vein and position the stimulating electrode in place in the chamber, it becomes quite difficult to remove or reposition the lead without possible severe trauma to surrounding tissue of the heart and/or the entry vein. This is a serious obstacle to even slight repositioning of the electrode once affixed, such as the surgeon might attempt if, as sometimes happens, the threshold for the anchored electrode is considerably higher than was observed just prior to the "permanent" fixation.
Accordingly, it is another object of the present invention to provide an active fixation mechanism for a catheter lead, which may be removed from one fixation location to another without serious injury to nearby or underlying tissue.